Apple, 1 medium: Fructose 10.74 g

Honey: Fructose 17.19 grams per 2 tablespoons

Barbecue Sauce: HFCS number 1 ingredient

Ingredients: High Fructose Corn Syrup, Vinegar, Concentrated Tomato Juice (Water, Tomato Paste), Water, Modified Food Starch, Salt, Honey, Contains Less Than 2% of Molasses, Natural Flavor, Paprika, Spice, Mustard Flour, Guar Gum, Red 40.

A1 Steak Sauce: HFCS number 2 ingredient

Ingredients: Tomato puree (water, tomato paste), high fructose corn syrup, vinegar, salt, water dried onions, contains less than 2% of black pepper, modified food starch, citric acid, dried parsley, dried garlic, xanthan gum, caramel color, potassium sorbate and calcium disodium EDTA as preservatives, molasses, corn syrup, sugar, spices, tamarind, natural flavor

Another in a series of data extrapolations that attempt to predict long-term cancer risk from medical radiation exposure was published in the July 13, 2009 Archives of Internal Medicine, viewable here.

Over the years, I've fussed about the radiation dose used by some centers for CT heart scans. (Note: I'm talking about CT heart scans, not CT coronary angiograms, an entirely different test with different radiation exposure.) In the "old" days, when electron-beam devices (EBT) were the best on the block, the old single-slice CT scanners (the predecessor of the current 64-slice MDCT scanners) exposed patients to ungodly quantities of radiation, while the EBT devices required very small quantities (0.5 mSv or about the equivalent of 4 standard chest x-rays or one mammogram).

But CT technology has advanced considerably. While EBT has been phased out (although it was an exceptional technology, GE acquired the small California manufacturer, then promptly scrapped the operation; you can guess why), multi-detector CT (MDCT) technology has improved in speed, image quality, and radiation exposure.

While it has improved, radiation exposure still remains an issue. The authors of the study applied the scanning protocols used at three hospitals and those in several CT heart scan studies, then calculated radiation exposure. They found a more than ten-fold range of exposure, from 0.8 mSv to 10.5 mSv. (All scanners were MDCT, none EBT.)

That's precisely what I've been worrying about: In the rapid rush to develop new devices, radiation exposure has often been a neglected issue. While some scan centers do an excellent job and take steps to minimize exposure, others barely lift a finger and consequently expose their patients to unnecessary radiation.

However, it's not as bad as it sounds. For one, the study included 16-slice MDCT scanners, a scanner type that I warned people to not use because of radiation. On the current most popular 64-slice devices, much lower radiation exposure is possible, on the order of 0.8-1.2 mSv routinely--if the center takes the effort.

This study, while eye-opening, will achieve some good: CT heart scans are here to stay. But the day-to-day practice of heart scanning should be:

1) standardized
2) conducted with radiation exposure as low as possible, preferably <0.8 mSv

To read more about this issue, below I've reprinted a 2007 full Track Your Plaque Special Report, CT Heart Scans and Radiation: The Real Story.

CT heart scans and radiation: The real story

“My personal opinion is that many patients today who are receiving multiple CT scans may well be getting at least comparable doses to subjects that have now developed malignancies from x-ray radiation received in the 1930s and '40s. And, similar to those days when the doses were unknown, the dose that patients receive today over a course of years of multiple CT scans is also completely unknown . . .

“I recommend that all healthcare providers become familiar with the concept that 1 in 1000 CT studies of the chest, abdomen, or pelvis may result in cancer.”

Richard C. Semelka, MD

Professor and Vice Chairman, Department of Radiology

University of North Carolina–Chapel Hill

Is this just hype to generate headlines? Or is the truth buried in the enormous marketing clout of the medical device industry, among which the imaging device manufacturers reign supreme?

It’s been over 110 years since radiation was first used for medical imaging. Over those years, it has had its share of misadventures.

In the 1930s and 1940s, before the dangers of radiation were recognized, shoe shoppers had shoes fitted using an x-ray device of the foot to assess fit. High doses of radiation were used to shrink enlarged tonsils and extinguish overactive thyroid glands. Attitudes towards radiation were so lax that doctors commonly permitted themselves to be exposed without protection day after day, year after year, until an unexpected rise in blood cancers like leukemia was observed. As recently as the 1970s and 1980s, cancers like Hodgkins’ disease were treated with high doses of radiation, also leading to radiation-induced diseases decades later.

Not all radiation is bad. Radiation can also be used as a therapeutic tool and even today remains a useful and reasonably effective method to reduce the size, sometimes eliminate, certain types of cancer. Forty percent of people with cancer now receive some form of radiation as part of their treatment (Ron E 2003).

Just how much does medical radiation add to our exposure?

Estimates vary, but most experts estimate that medical imaging provides approximately 15% of total lifetime exposure. In other words, radiation exposure from medical imaging is simply a small portion of total exposure that develops over the years of life. Exposure can be much higher, however, in a specific individual who undergoes repeated radiation imaging or treatment of one sort or another.

For all of us, exposure to medical radiation is part of lifetime exposure from multiple sources, added to the radiation we receive from the world around us. Just by living on earth, we are exposed to radiation from space and naturally-occurring radioactive compounds, and receive somewhere around 3.0 mSv per year (U.S. Nuclear Regulatory Commission). (Doses for radiation exposure are commonly expressed in milliSieverts, mSv, a measure that reflects whole-body radiation exposure.) People living in high-altitude locales like Colorado get exposed to an additional 30–50% ambient radiation (1.0–1.5 mSv more per year).

Much of the information on radiation exposure comes from studies like the Life Span Study that, since 1961, has tracked 120,000 Japanese exposed to radiation from the atomic bombs dropped in 1945 (Preston DL et al 2003). Although regarded as a high-dose exposure study for obvious reasons, there are actually thousands of people in this study who were exposed to lesser quantities of radiation (because of distance from the bomb sites) who still display a “dose-response” increased risk for cancer many years later in life. Radiation exposures of as little as 5–20 mSv showed a slight increase in lifetime risk.

Occupational and excessive medical exposure to radiation also provides a “laboratory” to examine radiation risk. Miners exposed to radon gas; patients exposed to the imaging agent, Thorotrast, containing radioactive isotope thorium dioxide and used as an x-ray contrast agent in the 1930s and 1940s and possesses the curious property of lingering in the body for over 30 years after administration; radium injections administered between 1945 and 1955 to treat diseases like ankylosing spondylitis and tuberculosis, all provide researchers an opportunity to study the long-term effects of various types of radiation exposure over many years (Harrison JD et al 2003).

The excess exposure of workers and several hundred thousand nearby residents to the Mayak nuclear plant in Russia has also revealed a “dose-response” relationship, with increasing exposure leading to more cancers, including leukemia and solid cancers of the bone, liver, and lung (Shilnikova NS et al 2003). Nuclear waste released into the Techa river between 1948 and 1956 contaminated drinking water used by over 100,000 Russians. A plant explosion in 1957 also released an excess of radiation into the atmosphere, yielding exposure via inhalation. Some sources estimate that at least 272,000 people have been affected by radiation from the Mayak plant. This unfortunate situation has, however, yielded plenty of data on radiation exposure and its long-term effects.

It’s also been known for several decades that people who receive therapeutic radiation for treatment of cancer, even with the reduced doses now employed, are subject to increased risk of a second cancer consequent to the radiation treatment.

From experiences like this, radiation experts estimate that an exposure of 10 mSv increases a population’s risk for cancer by 1 in 1000 (Semelka RC et al 2007).

This question was recently thrust into the spotlight with publication of a study from Columbia University in New York suggesting that a 20-year old woman would be exposed to a lifetime risk of cancer as high as 1 in 143 consequent to the radiation received during a CT coronary angiogram. (Important note: This was estimated risk from a CT coronary angiogram, not a simple heart scan that we advocate for the Track Your Plaque program.) The risk at the low end of the spectrum would be in an 80-year old man (because of the shorter period of time to develop cancer), with a risk of 1 in 5017. If “gating” to the EKG is added (which many scan centers do indeed perform nowadays), risk for a 60-year old woman is estimated at 1 in 715; risk for a 60-year old male, 1 in 1911 (Einstein AJ et al 2007). This study generated some criticism, since it did not directly involve human subjects, but used “phantoms” or x-ray dummies to simulate x-ray exposure. Nonetheless, the point was made: CT coronary angiograms in current practice do indeed expose the patient to substantial quantities of radiation, sufficient to pose a lifetime risk of cancer.

The media frenzy

The NY Times ran an article called With Rise in Radiation Exposure, Experts Urge Caution on Tests in which they stated:

"According to a new study, the per-capita dose of ionizing radiation from clinical imaging exams in the United States increased almost 600 percent from 1980 to 2006. In the past, natural background radiation was the leading source of human exposure; that has been displaced by diagnostic imaging procedures, the authors said."

“This is an absolutely sentinel event, a wake-up call,” said Dr. Fred A. Mettler Jr., principal investigator for the study, by the National Council on Radiation Protection. “Medical exposure now dwarfs that of all other sources.”

Radiation is a widely used imaging tool in medicine. Although CT scans of the brain, bones, chest, abdomen, and pelvis account for only 5% of all medical radiation procedures, they are responsible for nearly 50% of medical radiation used. It’s been known for years that increasing radiation exposure increases cancer risk over many years, but the boom of newer, faster devices that provide more detailed images has opened the floodgates to expanded use of CT scanners.

But before we join in the hysteria, let's first take a look at exposure measured for different sorts of tests:

Typical effective radiation dose values for common tests

Computed Tomography

Head CT 1 – 2 mSv
Pelvis CT 3 – 4 mSv
Chest CT 5 – 7 mSv
Abdomen CT 5 – 7 mSv
Abdomen/pelvis CT 8 – 11 mSv
Coronary CT angiography 5 – 12 mSv

Non-CT

Hand radiograph Less than 0.1 mSv
Chest radiograph Less than 0.1 mSv
Mammogram 0.3 – 0.6 mSv
Barium enema exam 3 – 6 mSv
Coronary angiogram 5 – 10 mSv
Sestamibi myocardial perfusion (per injection) 6 – 9 mSv
Thallium myocardial perfusion (per injection) 26 – 35 mSv

Source: Cynthia H. McCullough, Ph.D., Mayo Clinic, Rochester, MN

A plain, everyday chest x-ray, providing less than 0.1 mSv exposure, provides about the same quantity of radiation exposure as flying in an airplane for four hours, or the same amount of radiation from exposure to our surroundings for 11–12 days. Similar exposure arises from dental x-rays.

If you have a heart scan on an EBT device, then your exposure is 0.5-0.6 mSv, roughly the same as a mammogram or several standard chest x-rays.

With a heart scan on a 16- or 64-slice multidetector device, exposure is ideally around 1.0-2.0 mSv, about the same as 2-3 mammograms, though dose can vary with this technology depending on how it is performed (gated to the EKG, device settings, etc.)

CT coronary angiography presents a different story. This is where radiation really escalates and puts the radiation exposure issue in the spotlight. As Dr. Cynthia McCullough's chart shows above, the radiation exposure with CT coronary angiograms is 5-12 mSv, the equivalent of 100 or more chest x-rays or 20 mammograms. Now, that's a problem.

The exposure is about the same for a pelvic or abdominal CT. The problem is that some centers are using CT coronary angiograms as screening procedures and even advocating their use annually. This is where the alarm needs to be sounded. These tests, as wonderful as the information and image quality can be, are not screening tests. Just like a pelvic CT, they are diagnostic tests done for legitimate medical questions. They are not screening tests to be applied broadly and used year after year.

It’s also worth giving second thought to any full body scan you might be considering. These screening studies include scans of the chest, abdomen, and pelvis. These scans, performed for screening, expose the recipient to approximately 10 mSv of radiation (Radiological Society of North American, 2007). Debate continues on whether the radiation exposure is justified, given the generally asymptomatic people who generally undergo these tests.

Always be mindful of your radiation exposure, as the NY Times article rightly advises. However, don't be so frightened that you are kept from obtaining truly useful information from, for instance, a CT heart scan (not angiography) at a modest radiation cost.

Heart scans, CT coronary angiograms and the future

Unfortunately, practicing physicians and those involved in providing CT scans are generally unconcerned with radiation exposure. The majority, in fact, are entirely unaware of the dose of radiation required for most CT scan studies and unaware of the cancer risk involved. It is therefore up to the individual to insist on a discussion of the type of scanner being used, the radiation dose delivered (at least in general terms), the necessity of the test, alternative methods to obtain the same diagnostic information, all in the context of lifetime radiation exposure.

Our concerns about radiation exposure all boil down to concern over lifetime risk for cancer, a disease that strikes approximately 20% of all Americans. Many factors contribute to cancer risk, including obesity, excessive saturated fat intake, low fiber intake, lack of vitamin D, repeated sunburns, excessive alcohol use, smoking, exposure to pesticides and other organochemicals, asbestos and other industrial exposures, electromagnetic wave exposure, and genetics. Radiation is just one source of risk, though to some degree a controllable one.

Some people, on hearing this somewhat disturbing discussion, refuse to ever have another medical test requiring radiation. That’s the wrong attitude. It makes no more sense than wearing lead shielding on your body 24 hours a day to reduce exposure from the atmosphere. Taken in the larger context of life, radiation exposure is just one item on a list of potentially harmful factors.

It is, however, worth some effort to minimize radiation exposure over your lifetime, particularly before age 60, and by submitting to high-dose testing only when truly necessary, or when the potential benefits outweigh the risks. Thus, with heart scans and CT coronary angiography, some thought to the potential benefits of knowing your score or the information gained from the CT angiogram need to be considered before undergoing the test. Often the practical difficulty, of course, is that your risk for heart disease simply cannot be known until after the test.

In our view, in the vast majority of instances a simple CT heart scan can serve the simple but crucial role of quantifying risk for heart attack and atherosclerotic plaque. CT heart scans yield this information with less than a tenth of the radiation exposure of a CT coronary angiogram. In people without symptoms and a normal stress test, there is rarely a need for CT coronary angiography with present day levels of radiation exposure. Perhaps as technology advances and the radiation required to generate images is reduced, then we should reconsider.

Early experiences are suggesting that the newest 256-slice scanners, now being developed but not yet available, will cut the dose exposure of 64-slice CT angiograms in half (from 27.8 mSv to 14.1 mSv in a recent Japanese study). The 256-slice scanners will allow scanning that is faster over a larger area in a given period of time.

Thankfully, the scanner manufacturers are increasingly sensitive to the radiation issue and have been working on methods to reduce radiation exposure. However, it still remains substantial.

References:
Einstein AJ, Henzlova MJ, Rajagopalan S. Estimating risk of cancer associated with radiation exposure from 64-slice computed tomography coronary angiography. JAMA 2007 Jul 18;298(3):317–323.

Harrison JD, Muirhead CR. Quantitative comparisons of cancer induction in humans by internally deposited radionuclides and external radiation. Int J Radiat Biol 2003 Jan;79(1):1–13.

Hausleiter J, Meyer T, Hadamitzyky M et al. Radiation Dose Estimates From Cardiac Multislice Computed Tomography in Daily Practice: Impact of Different Scanning Protocols on Effective Dose Estimates. Circulation 2006;113:1305–1310.

Kalra MK, Maher MM, Toth TL, Hamberg LM, Blake MA, Shepard J, Saini S. Strategies for CT radiation dose optimization. Radiology 2004;230:619–628.

Mayo JR, Aldrich J, Müller NL. Radiation exposure at chest CT: A statement of the Fleischner Society. Radiology 2003; 228:15–21.

Mori S, Nishizawa K, Kondo C, Ohno M, Akahane K, Endo M. Effective doses in subjects undergoing computed tomography cardiac imaging with the 256-multislice CT scanner. Eur J Radiol 2007 Jul 10; [Epub ahead of print].

Preston DL, Pierce DA, Shimizu Y, Ron E, Mabuchi K. Dose response and temporal patterns of radiation-associated solid cancer risks. Health Phys 2003 Jul;85(1):43–46.

Ron E. Cancer risks from medical radiation. Health Phys 2003 Jul;85(1):47–59.

Shilnikova NS, Preston DL, Ron E et al. Cancer mortality risk among workers at the Mayak nuclear complex. Radiation Res 2003 Jun;159(6):787–798.

Semelka RC, Armao DM, Elias J Jr, Huda W. Imaging strategies to reduce the risk of radiation in CT studies, including selective substitution with MRI. J Magn Reson Imaging 2007 May;25(5):900–9090.

Copyright 2007, Track Your Plaque.

A carefully-conducted study by a collaborative research group at University of California-Berkeley has finally closed the lid on the fuss over fructose vs. glucose and its purported adverse effects.

The study is published in its entirety here.

Compared to glucose, fructose induced:

1) Four-fold greater intra-abdominal fat accumulation--3% increased intra-abdominal fat with glucose; 14.4% with fructose. (Intraabdominal fat is the variety that blocks insulin responses and causes diabetes and inflammation.)

2) 13.9% increase in LDL cholesterol but double the increase for Apoprotein B (an index of the number of LDL particles, similar to NMR LDL particle number).

3) 44.9% increase in small LDL, compared to 13.3% with glucose.

4) While glucose (curiously) reduced the net postprandial (after-eating) triglyceride response (area under the curve, AUC), fructose increased postprandial triglycerides 99.2%.

The authors propose that fructose specifically increases liver VLDL production, the lipoprotein particle that yields abnormal after-eating particles, increased LDL, and provides building blocks to manufacture small LDL particles. The authors also persuasively propose that fructose metabolism, unlike glucose, is not inhibited (via feedback loop) by energy intake, i.e., it's as if you are always starving.

Add to this the data that show that fructose increases uric acid (that causes gout and may act as a coronary risk factor), induces leptin resistance, causes metabolic syndrome (pre-diabetes), and increases appetite, and it is clear that fructose is yet another common food additive that, along with wheat, is likely a big part of the reason Americans are fat and diabetic.

Fructose is concentrated, of course, in high-fructose corn syrup, comprising anywhere from 42-90% of total weight. Fructose also composes 50% of sucrose (table sugar). Fructose also figures prominently in many fruits; among the worst culprits are raisins (30% fructose) and honey (41% fructose).

Also, beware of low-fat or non-fat salad dressings (rich with high-fructose corn syrup), ketchup, beer, fruit drinks, fruit juices, all of which are rich sources of this exceptionally fattening, metabolism-bypassing, LDL cholesterol/small LDL/ApoB increasing compound. Ironically, this means that many low-fat foods meant to reduce cholesterol actually increase it when they contain fructose in any form.

When you hear or say "fructose," run the other way, regardless of what the Corn Refiners Association says.

Matt came to me because his doctor couldn't reduce his LDL cholesterol.

His doctor had prescribed Zocor (simvastatin), Lipitor, Crestor, even pravastatin, all of which resulted in incapacitating muscle aches and weakness within a week of starting. No surprise, Matt had a jaundiced view of statin drugs.

We started out by characterizing his lipoprotein patterns:

--LDL 155 mg/dl

--72% of LDL was small LDL, a moderately severe pattern. (This means that small LDL comprised 112 mg/dl of the total 155 mg/dl LDL; large LDL comprised 43 mg/dl--small LDL was the problem.)

--HDL 42 mg/dl --Triglycerides 133 mg/dl

--No lipoprotein(a)

Beyond lipoproteins, Matt proved severely deficient in vitamin D with a starting level of 18 ng/ml.

Matt's doctor had advised that he avoid salt, as his blood pressure had been borderline high. His thyroid assessment disclosed a TSH of 3.89 mIU/ml with thyroid hormones free T3 and free T4 in the lower half of the normal range.

I therefore asked Matt to:

--Eliminate wheat, cornstarch, and sugars to reduce small LDL
--Add iodine
--Supplement 6000 units of an oil-based vitamin D preparation
--Take fish oil to provide at least 1800 mg EPA + DHA per day
--Take Armour Thyroid 1 grain per day

Several months later on this program, Matt had a repeat basic lipid panel:

--LDL 82 mg/dl--a 47% reduction

--HDL 52 mg/dl a 24% increase

--Triglycerides 60 mg/dl--a 55% decrease

In addition, vitamin D was 66 ng/ml, TSH was <1.0 mIU/ml with free T3 and free T4 in the upper half of the "reference range." Matt also felt great.

While the numbers could be slightly better, Matt had made tremendous progress towards achieving perfect values.

There you have it: Marked correction of cholesterol values, no statin drugs involved.

Even if you’re not interested in building big muscles like a bodybuilder, there are health benefits to increasing muscle mass: increased bone density, better balance, and fewer injuries. Greater muscle mass means higher metabolic rate, improved insulin responsiveness, lower blood sugar. The inevitable loss of muscle mass of aging can lead to frailty, an increasingly common situation for the elderly. Muscle loss be reversed, health improved as a result.

Since its introduction in 1994, creatine has exploded in popularity, particularly among bodybuilders and athletes interested in gaining muscle mass and strength. But creatine is not just for young weight lifters. If you are just interested in increasing muscle mass for its health benefits, then creatine is something to consider.

A study of creatine supplementation in men, average age 70 years, demonstrated that, when creatine was combined with strength training, it increased muscle mass 250% better than placebo (7.26 lb muscle vs 2.86 lb muscle), along with improved leg strength and endurance. The same group also demonstrated 3.2% increased bone density (measured using dual energy X-ray absorptiometry) after 12 weeks in participants taking creatine with strength training, while the control (no strength training, no creatine) group decreased by 1.0%.

Benefits are not confined to men. Similar results were observed in another study that included women (age 65 and older), with outcomes in females comparable to males. This is especially important for females, given the common development of osteopenia and osteoporosis in postmenopausal females.

Other studies have shown that benefits are maintained after stopping creatine supplementation.

The most popular form of creatine is the monohydrate, generally taken as a “loading” phase of 15-20 grams per day (generally split into 3-4 doses of 5 grams) for 5-7 days, followed by weeks to months of 2-5 grams per day.

An alternative form, polyethylene glycosylated creatine (PEG-creatine) provides similar effects at one-fourth to one-half the dose of creatine, i.e., 1.25-2.5 grams per day.

Despite previous concerns about kidney toxicity with prolonged use, another study showed that athletes taking creatine for up to 21 months have shown no adverse effects on kidney function, lipid (cholesterol) values, or other basic health measures.

Having healthy muscle mass doesn't make you bulge like a bodybuilder. With modest efforts at strength training, augmented with creatine supplementation, you have a wonderful tool to feel better, reduce injury, increase bone density, and combat abnormal insulin resistance, not to mention accelerate weight loss, since lean muscle mass consumes energy.

There has been a lot of debate over whether or not “bio-identical” hormones, i.e., hormones identical to the human form, are superior to non-human forms dispensed by the drug industry.

The FDA is currently taking steps to clamp down on availability of bioidentical hormones and their claims of superiority, despite a groundswell of grassroot support for them. The argument has pitted anti-aging practitioners and the public, as well as the likes of Oprah and Suzanne Somers, against Big Pharma and the FDA, the two forces trying to squash the bioidentical hormone movement.

Regardless of what heavy-handed approach the FDA takes, we already have access to hormones identical to the original human form. It requires no prescription and yields downstream hormones that the human body recognizes as human.

That "bioidentical" hormone is pregnenolone.

Pregnenolone is the first biochemical step in the conversion of dietary cholesterol (yes-cholesterol!) to numerous other hormones. Pregnenolone is the source of the hormones that lie at the center of the bioidentical hormone controversy: estrogens, progesterone, and testosterone. We therefore already have our own over-the-counter, non-prescription form of bioidentical hormones.

Supplemental pregnenolone increases estrogens (mildly), progesterone, and testosterone. Prenenonlone supplementation simply provide more of the basic substrate for hormone production. The increase in hormones is usually modest, not as vigorous as direct hormone replacement like, say, testosterone or progesterone topical creams. But pregnenolone can be useful when small to moderate increases are desired, such as for reduction of Lp(a). A theoretical downside is that pregnenonlone can also convert to cortisol, the adrenal gland hormone that regulates fluid and blood pressure. However, I've not seen any measurable increase in cortisol with low doses of pregnenonlone and limited data suggest that it does not. Pregnenolone also converts to the other adrenal gland hormone, DHEA; I call DHEA "the hormone of assertiveness," since some people who take too much pregnenolone (or direct DHEA) acquire excessive assertiveness.

The key to pregnenolone supplementation is to proceed gradually and begin with a small dose, e.g., 5 mg every morning. Hormonal assessment is best conducted periodically to assess the effects and to determine whether a dose adjustment is in order.

Heart Scan Blog reader, Roger, described his near-miss experience with CT coronary angiograms.

Hoping to obtain just a simple CT heart scan, he was bullied to get a CT coronary angiogram instead. Roger held strong and just asked for the test that we all should be having, a CT heart scan.

I posted yesterday that I was about to have my first CT heart scan...well, it was an interesting experience for reasons I coudn't possibly have anticipated. Dr. Davis has commented in the past on the confusion in the media about the difference between a CT calcium score scan, and a CT angiography, the latter requiring a far higher dose of radiation. I assumed this was a source of confusion only among patients and lay folks, but, lo and behold, I discovered today that doctors--or at least their helpers--can be just as confused.

Here's my story:

After checking in, I asked the receptionist to see if she had any information on whether my medical insurance was covering the scan. She called someone, and I heard her say over the phone, "He's here for a CT angiogram." At that point my ears perked up. I explained I wasn't here for a CT angiogram, only a regular CT scan. "Well, do you want to call your doctor and talk about this?" she asked. No, I said, I would like to ask one of their folks to verify exactly what test my doctor had ordered. As luck would have it, the technician was walking by at that point. "Is this a CT angiogram?" the receptionist asked. "No, it's just a CT calcium score scan" was the reply. But apparently the technician had been unclear herself, and had called my doctor just to verify. In other words, the "default" procedure they were accustomed to doing at this august Houston vascular clinic was a CT angiogram.

In fact, my appointment was even listed on their calendar as a "CT angiogram." For all I know, my insurance will be billed for the same. Later, during the procedure, the technician acted surprised I wasn't doing the "full test." I explained I had minimal risk factors (actually only one, an HDL of 34 a couple of years ago, which has since been raised to 50 partly as a result of taking advice from this site), but that my doctor was progressive (he is an MD for the Houston Astros) and thought it was a good idea since there is heart disease in my immediate family. My doctor did indeed prescribe only a CT calcium score scan, but it seems to have been an order that this clinic, at least, wasn't all that used to seeing.

So, I guess the message is: we have a lot of educating to do. Had I not been a faithful reader of these pages, I certainly wouldn't have known what kind of test I was about to get, or what questions to ask!

As for the heart scan itself, a piece of cake. If you can hold your breath, you can take this test. Just be sure it is the right one!

Why the "push" towards CT coronary angiograms and not "just" a CT heart scan? Well, I know it's shocking but it's . . . money!

CT coronary angiograms yield around $1800-$4000 per test. CT heart scans yield somewhere around $200. Though the scan center support staff might not care too much about the money themselves, their administrators likely make the cost distinctions clear to them.

Another reason: Most scan center staff, ironically, don't understand what a heart scan means, nor do they understand how it might serve to launch a program of prevention. They do understand that severe blockage by CT angiogram "needs" to be stented or bypassed. So they push patients towards things they understand.

Nobody makes money from CT heart scans, just as nobody makes money from a mammogram. Heart scans also don't lead to heroic, "lifesaving" procedures. They just lead to this sleepy, unexciting, inexpensive thing called prevention.

The June 20-21, 2009 Wall Street Journal Weekend Journal featured a provocative front page article written by physician, Dr. Abraham Verghese:

The Myth of Prevention

While eloquently written, I took issue with a few crucial points. Here is the letter I sent to the Editor at Wall Street Journal:

Dear Wall Street Journal Editor,

Re: Dr. Abraham Verghese’s article, The Myth of Prevention in the June 20-21, 2009 Weekend Journal.

I believe a more suitable title for Dr. Verghese’s article would be: “The Myth of What Passes as Prevention.”

As a practicing cardiologist, I, too, have witnessed firsthand the systemic “corruption” described by Dr. Verghese, the doing things “to” people rather than “for” them. Heart care, in particular, is rife with this form of profit-driven health delivery.

There is a fundamental flaw in Dr. Verghese’s otherwise admirable analysis: He assumes that what is called “prevention” in mainstream medicine is truly preventive.

Dr. Verghese makes issue of the apparent minor differences between preventing a condition and just allowing a condition to run its course. Prostate cancer screening is one example: Men subjected to repeated screenings have little length-of-life advantage over men who just allow their prostate to suffer the expected course of disease.

What if, instead, “prevention” as practiced today is nothing more than a solution that has been adopted in mainstream practice to suit yet another doing “to” strategy than doing “for”? In the prostate cancer example, PSA and prostate exam screenings often serve as little more than a means of harvesting procedures for the local urologist.

That’s not prevention. It is a prototypical example of “prevention” being subverted into the cause of revenue-generating procedures.

I submit that Dr. Verghese has fallen victim to the very same system he criticizes. His views have unwittingly been corrupted by the corrupt profit-driven system he describes.

What if, instead, prevention were just that: prevention or elimination of the condition. What if “prevention” of prostate cancer eliminated prostate cancer? What if heart disease “prevention” prevented all heart disease? What if this all proceeded without regard for profit or revenue-generating procedures, but just on results?

Dr. Verghese specifically targets heart scans or coronary calcium scoring, a test he likens to “miracle glow-in-the-dark minnow lures,” calling them “moneymakers.” Yes, when subverted into a corrupt algorithm of stress test, heart catheterization, stent, or bypass, heart scans are indeed a test used wrongly to “prevent” heart disease.

But what if the risk insights provided by heart scans prompt the start of a benign yet effective “prevention” program that inexpensively, safely, and assuredly prevents--in the true sense of the word--or eliminates heart disease? Then I believe the differences in mortality, quality of life, and costs would be substantial. Such strategies exist, yet do not necessarily include prescription drugs and certainly do not include the aftermath of heart catheterization and bypass surgery. Yet such programs fail to seize the limelight of media attention with no new high-tech lifesaving headline nor a big marketing budget to broadcast its message.

The problem in medicine is not prevention and its failure to yield cost- and life-saving results. It is the pervasively profit-driven mindset that keeps true preventive strategies from entering mainstream conversation. It is a repeat of Dr. Ignaz Semmelweis’ late 19th-century pleads for physicians to wash their hands before delivering babies to reduce puerperal sepsis, ignominious advice that earned him life and death in an asylum. We are essentially continuing to deliver children with unwashed hands because there is no revenue-generating procedure to clean them.

No, Dr. Verghese, the economic and medical failings of preventive strategies are not at fault. The failure of the medical system, in which everyone is bent on seizing a piece of the financial action for himself, has resulted in the failure to support the propagation of true preventive strategies that could genuinely save money and lives.

President Obama’s goal of cultivating preventive practices in medicine can work, but only if the profit-motive for “prevention” does not serve as the primary determinant of practice. Results-driven practices that are applied without regard to profit have the potential to yield the sorts of cost-saving and life-saving results that can reduce healthcare costs.

William Davis, MD
Milwaukee, Wisconsin
Medical Director, The Track Your Plaque Program (www.cureality.com)
Blog: http://heartscanblog.blogspot.com

The efforts of Texas House of Representatives Rep. Rene Oliveira and the SHAPE Guidelines committee have paid off: The Texas legislature passed a bill that requires health insurers to cover CT heart scans.

(NOTE: Don't make the same mistake that the media often makes and confuse CT heart scans with CT coronary angiography: two different tests, two different results, two different levels of radiation exposure. The difference is discussed here.)

Track Your Plaque previously reported the release of the SHAPE Guidelines, an ambitious effort to open CT heart scanning to people who would benefit from a simple screening test for coronary disease. Rep. Rene Oliveira initially introduced the bill in 2006, after having a heart scan uncovered extensive coronary plaque that resulted in coronary bypass surgery.

The bill requires that health-benefit providers cover the cost of CT heart scans (and carotid ultrasound) in men between the ages of 45-76, women 55-76, as well as anyone with diabetes or at "intermediate-risk" or higher for coronary disease by Framingham risk score.

The usual panel of cardiology knuckleheads stepped to the media podium, expressing their incredulity that something as "unvalidated" as heart scans could gain the backing of legislative mandate. Heartwire carried this comment:

"Contacted by heartwire, Dr Amit Khera (University of Texas Southwestern Medical Center, Dallas) confirmed there are still no comprehensive, adequately powered studies showing that these screening tests lead to better outcomes. In a phone interview, Khera said he has major concerns about how physicians will use these tests, particularly primary-care physicians. "I gave a talk last week to primary-care doctors, and there were probably 250 people in the room, and when I asked how many people had ordered a calcium scan, just one person raised a hand. . . . Most people don't even know what to do with the Framingham risk score, so they're going to follow an algorithm that they don't know how to follow to order a test result that they don't know what to do with."

It's the same criticisms hurled at heart scans over the years despite literally thousands of studies validating their application.

Studies have conclusively shown that:

--Coronary calcium scores generated by a CT heart scan outperform any other risk measure for coronary disease, including LDL cholesterol, c-reactive protein, total cholesterol, HDL cholesterol, blood pressure.
--Coronary calcium scores yield a graded, trackable index of coronary risk. Scores that increase correlate with increased risk of cardiovascular events; scores that remain unchanged correlate with much reduced risk.
--A coronary calcium score of zero--no detectable calcium--correlates with extremely low 5-year risk for cardiovascular events.
--Coronary calcium scores correlate with other measures of coronary disease. Heart scans correlate with coronary angiography, quantitative coronary angiography, carotid ultrasound (intimal-medial thickness and plaque severity), ankle-brachial index, and stress tests, including radionuclide (nuclear) perfusion imaging.

The reluctance of my colleagues to embrace heart scans stems from two issues, for the most part:

1) No study has yet been performed showing that knowing what the score is vs. not knowing what the score is changes prognosis. That's true. But it is also true of the great majority of practices in medicine. While many wrongs don't make a right, the miserable and widespread failure of other coronary risk measures, like LDL cholesterol or c-reactive protein, to readily and reliably detect hidden coronary disease creates a gaping void for improved efforts at early detection. If your LDL cholesterol is 140 mg/dl, do you or don't you have coronary disease? If your doctor's response is "Just take a statin drug anyway" you've been done a great disservice. (If and when this sort of study gets done, its huge cost--outcome studies have to be large and last many years--it will likely be a statin study. It is unlikely it will include such Track Your Plaque strategies that help reduce heart scan scores, like vitamin D and correction of small LDL particles.)

2) Fears over overuse of hospital procedures triggered by heart scans. This is a legitimate concern--if the information provided by a heart scan is misused. Heart scans should never--NEVER--lead directly to heart catheterization, stents, bypass surgery. Heart scans do not change the indications for performing revascularization (angioplasty, stents, bypass). Just because 20% of my cardiology colleagues are more concerned with profit rather than patient welfare does not invalidate the value of the test. Just because the mechanic at the local garage gouged you by replacing a carburetor for $800 when all you need was a new spark plug does not mean that we should outlaw all auto mechanics. Abuse is the fault of the abuser, not of the tool used to exercise the abuse.

All in all, while I am not a fan of legislating behavior in healthcare, the blatant and extreme ignorance of this simple tool for uncovering hidden heart disease makes the Texas action a huge success for heart disease prevention. I hope that this success will raise awareness, not just in Texas, but in other states and cities in which similar systemic neglect is the rule.

Remember: CT heart scans are tools for prevention, not to uncover "need" for procedures. They serve as a starting point to decide whether or not an intensive program of prevention is in order, and I don't mean statin vs. no statin.

Though not a multi-million dollar statin drug study, I have NEVER seen a heart attack or "need" for procedure in any person who has stopped progression or reduced their heart scan score. A small cohort from my practice was reported:

Effect of a Combined Therapeutic Approach of Intensive Lipid Management, Omega-3 Fatty Acid Supplementation, and Increased Serum 25 (OH) Vitamin D on Coronary Calcium Scores in Asymptomatic Adults.

Davis W, Rockway S, Kwasny M.

The impact of intensive lipid management, omega-3 fatty acid, and vitamin D3 supplementation on atherosclerotic plaque was assessed through serial computed tomography coronary calcium scoring (CCS). Low-density lipoprotein cholesterol reduction with statin therapy has not been shown to reduce or slow progression of serial CCS in several recent studies, casting doubt on the usefulness of this approach for tracking atherosclerotic progression. In an open-label study, 45 male and female subjects with CCS of >/= 50 without symptoms of heart disease were treated with statin therapy, niacin, and omega-3 fatty acid supplementation to achieve low-density lipoprotein cholesterol and triglycerides /=60 mg/dL; and vitamin D3 supplementation to achieve serum levels of >/=50 ng/mL 25(OH) vitamin D, in addition to diet advice. Lipid profiles of subjects were significantly changed as follows: total cholesterol -24%, low-density lipoprotein -41%; triglycerides -42%, high-density lipoprotein +19%, and mean serum 25(OH) vitamin D levels +83%. After a mean of 18 months, 20 subjects experienced decrease in CCS with mean change of -14.5% (range 0% to -64%); 22 subjects experienced no change or slow annual rate of CCS increase of +12% (range 1%-29%). Only 3 subjects experienced annual CCS progression exceeding 29% (44%-71%). Despite wide variation in response, substantial reduction of CCS was achieved in 44% of subjects and slowed plaque growth in 49% of the subjects applying a broad treatment program.

Take a look at the results from the Heart Scan Blog's most recent reader poll (399 respondents):

How many hours do you sleep per night (on average)?

9 or more hours per night
15 (3.7%)

8-9 hours per night
72 (18%)

7-8 hours per night
152 (38.1%)

6-7 hours per night
111 (27.8%)

5-6 hours per night
38 (9.5%)

Less than 5 hours per night
11 (2.8%)

Like many issues in health, too much or too little of a good thing can present undesirable consequences.

Too much sleep: While psychologists and sleep researchers advise us that at least 9 hours are required to fully eliminate sleep "debt" and achieve optimal vigilance and mental performance, epidemiologic studies have shown increased mortality with this quantity of sleep.

Too little sleep: Getting less than 7 hours habituallly increases blood sugar, appetite, inflammatory measures, and encourages weight gain. Mortality is also increased, just as with sleeping too much. It is also associated with increased likelihood of a positive heart scan score.

7-8 hours per night from a health viewpoint is that Goldlilocks "just right" value: just enough to not erode mental performance substantially, but not so little that inflammatory, insulin-disrupting, and appetite-increasing effects develop.

Of our 399 respondents in the poll, 56.1% (38% + 18%) slept what appears to be an optimal amount for health. While only 3.7% slept too much (9 hours or more), the remaining 40.1% slept too little.

Our informal poll confirms what most of us observe in everyday life: The majority of people shortchange sleep in order to meet the demands of their high-pressure, squeeze-as-much-as-possible-into-every-day lives. But not paying off your sleep "debt" is like not paying the mortgage for a couple of months. You wouldn't expect your friendly neighborhood bank to say, "Oh, you forgot to pay your mortgage? Forget about it. Just pay next month's." Sure, fat chance. But if you don't pay off your sleep "debt," you will pay it back with health.

Lou was recovering from his 3rd bypass operation. This third go-round left him weaker, slower, less quick on the rebound. In fact, he was lucky to have survived.

At 71 years old, Lou went a good 15 years since his second bypass, another 10 years prior to his first bypass at age 46.

In the days immediately following Lou's bypass, I had a chance to talk to his son, who stayed at his Dad's bedside while Lou struggled through post-op recovery.

"Did your Dad tell you about why this has happened, what caused his heart disease?" I asked.

"Sort of. He just said I should get checked," Lou's son, Aaron, replied.

"Did he mention the lipoprotein(a) pattern he has?"

"No. He never mentioned anything like that. He just said to get checked."

That's how it gets played out more often than not: Mom or Dad has a heart attack, stents, or (3rd) bypass, the children are told to get checked. Getting "checked" assumes that the doctor knows what to check for.

In Lou's case, the reason why he was in the hospital getting his 3rd (and final) bypass was lipoprotein(a), along with genetically-determined small LDL particles, low HDL, a postprandial (after-eating) disorder, hypertension, and borderline diabetes, not to mention vitamin D deficiency, omega-3 fatty acid deficiency, and marginal thyroid function. (Lou, a retired city employee, had showed only marginal interest in correcting these patterns. While he accepted medications, he proved unwilling to engage in the diet and nutritional supplement strategies required to correct his patterns.)

So Lou's 3rd bypass operation provided a moment of reflection for Aaron to ask: "Could I share the fate of my Dad?" With Lou's combination of genetic patterns, there was at least a 75% likelihood that he did. Sadly, going to his doctor would likely yield little more than a cholesterol panel, a question about smoking, and a prescription for Lipitor.

Just getting "checked" would be, more than likely, a recipe for disaster for Aaron: heart disease in his 40s or 50s. That's why you need to take control over this sad state of affairs and ask--no, insist--that an effort be made to determine whether you might share your parents' fate.

"This diet works great," Don declared. "But I think I've lost too much weight."

At 67 years old and 5 ft. 11 inches, Don began the program weighing 228 lbs (BMI 31.9). Because of high triglycerides, high blood sugar, high c-reactive protein, and excessive small LDL, I instructed Don to eliminate all wheat products from his diet, along with cornstarch and sweets. His intake of lean meats, eggs, vegetables, oils, raw nuts, etc. was unlimited.

Don now weighed 194 lbs, down 34 lbs over 6 months (BMI 27.1). Triglycerides, blood sugar, blood pressure, and well-being had improved dramatically; small LDL, however, had dropped only 30%--still room for improvement.

"My friends say I'm too skinny. They ask if I have cancer!"

I've heard this many times: Someone loses weight in a relatively short period of time and friends and family tell you you're too skinny. "It must be cancer. Nobody loses weight like that."

Unfortunately, many Americans have forgotten what normal looks like. Normal is certainly not a 190-lb, 5 ft 4 in woman, nor is it a 228 lb, 5 ft 11 inch man. But Americans have put on so much weight that the prevailing view of what constitutes "normal" weight has been revised upward. Normal is closer to what we see in old movies from the 1940s and '50s with people like Jimmy Stewart and Donna Reed. That's what we are supposed to look like.

So Don actually remains mildly overweight but is judged as "too skinny," or even cancer-ridden, by friends and family.

Ignore such comments. As you lose pounds and approach a truly desirable weight, realize that you are returning to the normal state, not the vision of "normal" now held by most Americans.

Vitamin D is, without a doubt, the most incredible "vitamin"/prohormone/neurosteroid I have ever encountered. Frankly, I don't know how we got anything accomplished in health pre-D.

Unfortunately, people I meet rarely take their vitamin D in a way that accomplishes full restoration of vitamin D blood levels. It really isn't that tough.

Here's a list of common tripping points with vitamin D:

"I take vitamin D: 1000 units a day."
This is probably the most common mistake I see: Taking a dose that is unlikely to yield a desirable blood level. (We use 60-70 ng/ml of 25-hydroxy vitamin D as our target.) Most men and women require 6000 units per day to achieve this level. There is substantial individual variation, however, with an occasional person needing much more, a rare person requiring as little as 1000 units.

"I bought some vitamin D on sale. They were white tablets."
Time and again, patients in my office who initially have had successful vitamin D replacement, despite being reminded that only oil-based forms should be taken, switch to tablets. While they initially showed a 25-hydroxy vitamin D blood level, for instance, of 67 ng/ml on 8000 units per day with an oil-based capsule, they switch to a tablet form and the next blood level is 25 ng/ml. In other words, tablets are very poorly or erratically absorbed.

I have had people use tablets successfully, however, by taking their vitamin D tablets with a teaspoon of oil, e.g., olive oil. Oil is necessary for full absorption.

"I'm going to Florida. I'll stop my vitamin D because I'm going to lay in the sun."
Wrong. 90% of adults over 40 years old have lost the majority of their ability to activate vitamin D in the skin. A typical response might be an increase in blood level from 25 to 35 ng/ml--a 10 ng increase with a dark brown tan.

There is an occasional person who, with sun exposure, increases blood levels substantially. This can occur in both fair-skinned and dark-skinned people, though I've never seen it happen in an African-American person. The occasional person who maintains the ability to convert vitamin D with sun exposure, or young people, should seasonally adjust their vitamin D dose, e.g., 6000 units winter, 3000 units summer, or some other regimen that maintains desirable blood levels. You can see that monitoring blood levels (we check levels every 6 months for the first 2 years) is crucial: You cannot know what your vitamin D needs are unless you assess 25-hydroxy vitamin D levels.

"I drink plenty of milk. I don't think I need to take vitamin D."
Oh, boy. This is so wrong on so many levels.

First of all, no adult should be drinking plenty of cow's milk. (A discussion for another day.) Second of all, cow's milk averages 70 units of vitamin D, often the D2 form (ergocalciferol), per 8 oz. Even if the FDA-mandated 100 units per day were present, an average adult dose of 6000 units would require 60 glasses of milk per day. Can you say "diarrhea"?

Likewise, other food sources of vitamin D, such as fish (300-400 units per serving) and egg yolks (20 units per yolk), are inadequate. This makes sense: Humans are not meant to obtain vitamin D from food, but from sun exposure over a large body surface area. And this is a phenomenon that is meant to occur only in the youthful, ensuring that nature takes its course and us older folks get old and make way for the young (i.e., unless we intervene by taking vitamin D supplements).

"My doctor said that my vitamin D blood level was fine. It was 32 ng/ml."
Let's face it: By necessity, your overworked primary care physician, who manages gout, hip arthritis, migraine headaches, stomach aches, prostate enlargement, H1N1, depression, etc., is an amateur at nearly everything, expert in nothing. Nobody can do it all and get it right. Likewise vitamin D. The uncertain primary care physician will simply follow the dictates of the laboratory form that specifies "30-100 ng/ml" as the "normal" or "reference range." Unfortunately, the laboratory often quotes population distributions of a lab measure, not an ideal or desirable level.

To illustrate the folly of population distributions of a measure, imagine you and I want to know what women weigh. We go to a local mall and weigh several thousand women. We tally up the results and find that women weigh 172 lbs +/- 25 lbs (the mean +/- 2 standard deviations). (That's true, by the way.) Is that desirable? Of course it isn't. Population average or population distribution does not necessarily mean ideal or desirable.

"My husband's doctor said he should take 4000 units per day. So I just take the same dose."
That would be fine if all adults required the same dose. However, individual needs can vary enormously. A dose that is grossly insufficient for one person may be excessive for another. Once again, vitamin D dose needs can be individualized by assessing 25-hydroxy vitamin levels in the blood.

"I don't need to take vitamin D. I already take fish oil."
I suspect this mistaken belief occurs either because people confuse fish oil with cod liver oil, which does contain some vitamin D. (Cod liver oil is not the best source of vitamin D, mostly because of the vitamin A content; also a discussion for another time), or because they've heard that eating fish provides vitamin D. However, fish oil capsules do not contain vitamin D unless it is added, in which case it should be prominently and explicitly stated on the label.

"I don't have to take vitamin D. It's summer."
For most people I know, if it's a bright, sunny July day, where are they likely to be? In an office, store, or home--NOT lying in the sun with a large body surface area exposed. Also, most people expose no more than 5-10% of surface area in public. I doubt you cut the grass in a bathing suit. Because of modern indoor lifestyles and fashion, the majority of adults need vitamin D supplementation year-round.

I advise everyone that gelcap vitamin D is preferable. Some, though not all, liquid drop forms have also worked. Take a dose that yields desirable blood levels. And blood levels of 25-hydroxy vitamin D are ideally checked every 6 months: in summer and in winter to provide feedback on how much sun activation of D you obtain.

If your doctor is unwilling or unable to perform vitamin D testing, fingerstick vitamin D test kits can be obtained from Track Your Plaque.

My friend, Jimmy Moore of Living La Vida Low Carb, describes his thyroid experience here.

As Jimmy points out, he was looking for a way to jump-start a 50-lb weight loss. In my experience, low thyroid hormone levels ("hypothyroidism") are an exceptionally common cause for weight gain. Correcting even marginal hypothyroidism can facilitate weight loss, often resulting in 10 or more pounds of weight loss within the first month.

Unfortunately, Jimmy's thyroid hormone panel proved normal: TSH 1.3, thyroid hormones free T3 and free T4 in the mid- to upper-half of the reference range.

I say "unfortunately" because it is really an easy, inexpensive, and benign solution for losing weight. (I don't, of course, wish that Jimmy or anyone else develops a thyroid condition. But it really can provide gratifying weight loss results when thyroid function is low.) Jimmy might consider taking his oral temperature first thing in the morning as another means of assessing the adequacy of thyroid function.

Perhaps you will be luckier than Jimmy and have thyroid dysfunction that can be corrected and jump-start your weight loss program. Fingerstick thyroid test kits like the one Jimmy used are available here from Track Your Plaque.

Fat = triglycerides

In other words, eat fat, whether it's saturated, hydrogenated, polyunsaturated, or monounsaturated, and blood levels of triglycerides will go up over the next 6 hours. This remains true if there are carbohydrates in the meal, or if there are NO carbohydrates in the meal. It also remains true if you chronically consume fats.

While fats are the primary determinant of postprandial (after-eating) triglycerides, carbohydrates are the primary determinant of fasting triglycerides.

So, if your triglycerides are high on a fasting cholesterol (lipid) panel, it's most likely because you overconsume carbohydrates.

Thanks to cartoonist Eli Stein, who has generously allowed me to reprint his artwork on these pages. Mr. Stein has published his work in dozens of magazines and newspapers, including the Wall Street Journal, Barron's, and Good Housekeeping. More of his work can be found at Eli Stein Cartoons.

Humans have limited capacity to store carbohydrates. Beyond the glucose and glycogen in our blood and tissues, we have relatively little carbohydrate to draw from in time of energy need. That's why long-distance runners and triathletes have to carry sugar sources to keep blood sugar from plummeting.

Fat, of course, is different. We have virtually unlimited capacity to store energy as fat.

Because we have limited carbohydrate storage capacity, what can the body do with the excessive quantities of carbohydrates that Americans ingest? What becomes of a bagel for breakfast, wheat crackers for snacks, a whole wheat sandwich for lunch, pretzels, and whole wheat pasta that many people eat every day, not to mention the chips, soft drinks, and juices?

Excess carbohydrates are diverted to an interesting metabolic pathway called de novo lipogenesis (DNL). This refers to the liver's ability to make triglycerides from excessive carbohydrates in the diet. Triglycerides are packaged for release into the blood as VLDL. VLDL, in turn, interacts with other lipoproteins, creating small LDL particles, reduced HDL and smaller, less protective HDL. High VLDL will be measured on a standard cholesterol panel as higher triglycerides.

A University of California (Berkeley, San Francisco) group has done much of the work describing DNL.

A diet weighed towards carbohydrates, especially if 50% or greater calories are carbohydrate, is sufficient to provoke plenty of DNL, even in slender people. DNL is a big part of the reason why low-fat (and, thereby, high-carbohydrate) diets result in higher triglycerides. DNL really gets turned on many-fold if the carbohydrates are "simple," rather than "complex."

Overweight people, however, can demonstrate five-fold greater DNL even with lesser quantities of carbohydrate intake (e.g., 40% fat, 46% carbohydrate, 14% protein):

From Schwarz et al 2003. Mean (± SEM) fractional de novo lipogenesis in lean normoinsulinemic (NI), obese NI, and obese hyperinsulinemic (HI) subjects after 5 d of consuming a high-fat, low-carbohydrate diet and in different lean NI and obese HI subjects after 5 d of consuming a low-fat, high-carbohydrate diet. Values with different superscript letters are significantly different.

Excessive carbohydrates, a la standard low-fat diets, are good for nobody. The concept of de novo lipogenesis fills in a theoretical hole that now explains why people who eat carbohydrates have higher triglycerides, VLDL, and, eventually, insulin resistance and diabetes.

I previously posted Gretchen's postprandial diet experiment, in which she consumed a low-fat diet for a day, followed by a low-carbohydrate diet for a day. Grethen monitored blood glucose and triglycerides with fingerstick checks. (Blood glucose can be checked on any widely available glucose monitor; triglycerides can be monitored with the Cardiochek device.)

Let's now discuss what happened.

On the low-carb, high-fat day, there was an initial surge in triglycerides to 250 mg/dl late morning, followed by a secondary peak several hours following dinner. Because fat is mostly triglycerides, Gretchen's high-fat (sausage, bacon, butter, whole-fat yogurt) breakfast provided a large quantity of triglycerides that needed to be absorbed. This generally occurs over approximately 6 hours, varying depending on body weight, how accustomed you are to fat, activity level during the day, the kind of fat in the meal. The high content of saturated fat in Gretchen's high-fat breakfast likely caused the somewhat slower drop in triglycerides over approximately 7 1/2 hours.

As Gretchen herself had noted, triglycerides the following day were lower, a typical low-carb response. Blood sugar throughout showed only minor variation, with only small postprandial increases.

Thus, Gretchen experienced what we'd expect with a low-carb, high-fat diet: an initial high surge in triglycerides, followed by a decline in fasting levels, while blood sugar shows a normal contour.

Now, the more confusing low-fat experience:

Blood glucose makes a striking peak at 200 mg/dl after the low-fat breakfast of pasta and rice, in contrast to the low-carb breakfast. Triglycerides behaved very differently from the low-carb experiment: While there was no initial postprandial surge, there was a late surge developing 6-24 hours later. The late surge continued into the next day, with fasting levels the following morning (210 mg/dl) exceeding the starting triglyceride level (60 mg/dl).

The one potentially confusing aspect of all this is Gretchen's late rise in triglycerides on the low-fat diet. This phenomenon is due to something called de novo lipogenesis, or the liver's conversion of carbohydrates to triglycerides that occurs when an excessive carbohydrate load comes through diet. Because the human body cannot store anything beyond a minor quantity of carbohydrates (as glucose and glycogen), carbohydrates are converted to fats.

Another factor causing the late triglyceride increase is insulin resistance, given the high blood sugar response. When insulin resistance is present, the activity of the enzyme, lipoprotein lipase, is reduced. Less lipoprotein lipase activity allows slower VLDL degradation, allowing VLDL (and thereby triglycerides contained in VLDL) to "stack up" in the blood. Thus, the higher triglycerides late after eating and into the next morning.

One issue to be aware of: Acute responses can differ from chronic responses. In other words, had Gretchen had the luxury (and time and money) to conduct the experiment over, say, 4 weeks, rather than a single day, there would be somewhat different responses. The best data on this come from Dr. Jeff Volek of the University of Connecticut, in which 4 weeks of low-carbohydrate eating modify fasting and postprandial responses over time.

Several conclusions can be made from Gretchen's experience:

1) Low-carb, high-fat acutely generates extravagant postprandial triglyceride responses.
2) Low-fat causes a late triglyceride surge and higher fasting triglycerides.
3) Low-fat leads to high blood sugars and, by implication, diabetes.

Both the low-carb and the low-fat responses are undesirable, both leading to increased risk for heart disease. Which is worse? I believe that low-fat is more destructive, since it leads over time to both high triglycerides and diabetes, while low-carb/high-fat only leads to postprandial triglyceride surges, at least acutely.

How to best balance the responses to reduce risk for heart disease? That's a discussion for future.

Again, my thanks to Gretchen and the substantial amount of effort that went into generating these numbers. More of Gretchens' own writing can be found on her blogs:
http://wildlyfluctuating.blogspot.com
http://www.healthcentral.com/diabetes/c/5068

A Heart Scan Blog reader sent this fascinating description of his wheat-free adventure.

Whenever I discuss this notion of going wheat-free and the incredible health effects that develop, I invariably receive comments or emails saying something like "I eat wheat and feel fine. That can't be true." The problem is that not everybody needs to go wheat-free. 20-30% of people can include wheat in their diet and suffer little more than weight gain, some not at all.

But stories like Michael's (below) are commonplace in my experience. I've had many patients who, at first, refused to believe that wheat exposure might be the underlying cause for health struggles. But they finally give it a try and find that rashes, arthritis, acid reflux, irritable bowel symptoms, mood swings, anger, etc. are miraculously improved or gone.

Anyway, hear what Michael has to tell us:

Dr. Davis,

I want to thank you. I was browsing the web a while back and happened to stumble upon your blog post about wheat belly. The first thing that caught my attention was that I thought you had somehow gotten a photograph of me. The young man you posted an image of looked exactly like me. So I read what you had to say. After reading, I thought "Four weeks isn’t so bad. I think I can handle this."

It has now been nine weeks and all I can say is that I am completely amazed. Let me say first that twice in the past twenty years I have been tested for allergies. The first time I was tested I showed a slight reaction to Timothy Grass, but not enough to cause me any problems. The second testing I did not show a reaction to anything. So, I have always assumed that my chronic sinus problem were due to sensitivities to environmental pollutions. Now I am not so sure. I would like to list for you everything that has happened to me since I eliminated wheat from my diet.

1. I have lost a total of 12 pounds in the last 9 weeks.
2. I have lost 1 ¼ inches of belly fat
3. I have lost a tremendous amount of fat from my neck.
4. My entire life I have had problems with oily hair. I could wash my hair and three hours later I looked as if I hadn’t washed in a week. Now my hair stays clean and soft for two to three days without shampoo.
5. My hair was always flat and stringy. Now it has lots of body.
6. I used to have thick layers of dry skin on my scalp. It would come loose in chunks as large as a fingernail. That dry scalp is gone.
7. I used to have dry flaky skin that seemed to secrete oil. That no longer happens. My skin is now soft and smooth.
8. I have lived with bad acne for at least 35 years. Now it is hard to find a pimple on my body.
9. I have always had to fight dehydration. That is no longer a problem.
10. I used to drink two large cups of coffee every morning just to be able to function. I now have enough energy that I have eliminated caffeine from my diet.
11. I sleep more soundly than ever before and my dreams are clear and vivid.
12. My thought processes are more active and clear than they have ever been.
13. My chronic sinus issue is now a thing of the past.
14. I used to have problems with getting the “shakes” if I had gone more than a couple of hours without eating. It was as if I was suffering from low blood sugar. I would even be afraid that I would pass out. Now all I feel is hunger. I can go all day without eating and never feel in danger of losing consciousness.

Today is Thursday. This past Monday my wife and I were eating out and I ordered a burger without a bun. What I didn’t realize was that the burger would arrive covered in onion rings. I knocked the mountain of onion rings onto the plate but there were still a couple that were embedded in the cheese. I decided, what the hell, a couple of onion rings shouldn’t make that much of a difference. I will not make that mistake again anytime soon. Within 30 minutes I felt like there was a steel spike going through my left eye socket. I don’t remember ever being in that much pain. My sinuses were exploding. This morning, as I write this, I still feel the vestiges of that pain. Just enough that I know it is there. But after two and a half days, I am at least able to function again.

I owe you a debt of gratitude. You may have just saved my life. In the very least you have given me the means to improve my life in ways that I never thought possible.

Thank you so much,
Michael B.

Now, if wheat exposure can do that in Michael, what damage can it do in other people?

Personally, I previously experienced many of the same symptoms that Michael suffered, all gone with wheat elimination.

My advice: If you have any inkling that you might have a wheat sensitivity, make a New Year's resolution to stay wheat-free for 4 weeks and see whether you can feel any difference. Not everybody will, but many will be telling us about the dramatic health turnarounds they experienced.

Lipoprotein lipase can make the difference between having heart disease and not having it. Having sky-high triglycerides or normal triglycerides. It can mean dinner hanging around for over 12 hours in the bloodstream, rather than the usual 4-6 hours.

We use a lot of niacin in the Track Your Plaque program.

Niacin:

--Increases HDL and shifts HDL towards the large, protective fraction

--Reduces small LDL--In fact, niacin is the best treatment we have to reduce small LDL after wheat elimination and carbohydrate reduction.

--Reduces fasting and postprandial (after-eating) triglycerides

--Reduces heart attack risk by 20-28%--even as a sole agent.

But . . . niacin also triggers higher blood sugar because it partially blocks the effects of insulin (insulin "resistance").

While the net effect of niacin remains positive, the provocation of insulin resistance is not such a good thing. Can it be minimized or eliminated?

Yes, through exercise. Here's one interesting observation in obese (BMI 34.0), sedentary men given placebo, exercise, niacin (1500 mg Niaspan, once per day), or niacin + exercise:

From Plaisance et al 2008.

Blood was drawn following a high-fat meal challenge. (Yes, a high-fat challenge, not a carbohydrate challenge. In this study, there were only 17 grams carbohydrates in the test meal, but 100 grams fat. More on this in future.) Exercise consisted of walking for 50 minutes at a moderate pace one hour prior to the meal challenge.

You can see from the graph that exercise partially corrected the increased insulin level provoked by niacin.

Judging from this and other studies, exercise can help minimize the insulin-blocking effects of niacin. It doesn't take much, just moderate exercise for at least 30 minutes.

Adequate sleep can also help, since sleep deprivation is a potent trigger for insulin resistance, only worsened in the presence of niacin. Vitamin D supplementation to achieve desirable blood levels (which I define as 60-70 ng/ml) is also an effective means to minimize this effect.

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